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黑色素可保护脉络膜血管免受光毒性损伤。

Melanin protects choroidal blood vessels against light toxicity.

作者信息

Peters Swaantje, Lamah Thomas, Kokkinou Despina, Bartz-Schmidt Karl-Ulrich, Schraermeyer Ulrich

机构信息

Center of Ophthalmology, University of Tuebingen, Schleichstr. 12, D-72076 Tuebingen, Germany.

出版信息

Z Naturforsch C J Biosci. 2006 May-Jun;61(5-6):427-33. doi: 10.1515/znc-2006-5-620.

Abstract

Low ocular pigmentation and high long-term exposure to bright light are believed to increase the risk of developing age-related macular degeneration (ARMD). To investigate the role of pigmentation during bright light exposure, cell damage in retinae and choroids of pigmented and non-pigmented rats were compared. Pigmented Long Evans (LE) rats and non-pigmented (albino) Wistar rats were exposed to high intensity visible light from a cold light source with 140,000 lux for 30 min. Control animals of both strains were not irradiated. The animals had their pupils dilated to prevent light absorbance by iris pigmentation. 22 h after irradiation, the rats were sacrificed and their eyes enucleated. Posterior segments, containing retina and choroid, were prepared for light and electron microscopy. Twenty different sections of specified and equal areas were examined in every eye. In albino rats severe retinal damage was observed after light exposure, rod outer segments (ROS) were shortened and the thickness of the outer nuclear layer (ONL) was significantly diminished. Choriocapillaris blood vessels were obstructed. In wide areas the retinal pigment epithelium (RPE) was absent in albino rats after irradiation. In contrast, LE rats presented much less cell damage in the RPE and retina after bright light exposure, although intra-individual differences were observed. The thickness of the ONL was almost unchanged compared to controls. ROS were shortened in LE rats, but the effect was considerably less than that seen in the albinos. Only minimal changes were found in choroidal blood vessels of pigmented rats. The RPE showed certain toxic damage, but cells were not destroyed as in the non-pigmented animals. The number of melanin granules in the RPE of LE rats was reduced after irradiation. Ocular melanin protects the retina and choroid of pigmented eyes against light-induced cell toxicity. Physical protection of iris melanin, as possible in eyes with non-dilated pupils, does not seem to play a major role in our setup. Biochemical mechanisms, like reducing oxidative intracellular stress, are more likely to be responsible for melanin-related light protection in eyes with dilated lens aperture.

摘要

低眼部色素沉着和长期暴露于强光被认为会增加患年龄相关性黄斑变性(ARMD)的风险。为了研究色素沉着在强光暴露过程中的作用,比较了有色和无色大鼠视网膜和脉络膜中的细胞损伤情况。将有色的长 Evans(LE)大鼠和无色(白化病)Wistar 大鼠暴露于来自冷光源的 140,000 勒克斯高强度可见光下 30 分钟。两种品系的对照动物均未接受照射。动物的瞳孔被扩大以防止虹膜色素沉着吸收光线。照射后 22 小时,处死大鼠并摘除眼球。制备包含视网膜和脉络膜的后部节段用于光学显微镜和电子显微镜检查。每只眼睛检查 20 个指定且面积相等的不同切片。在白化病大鼠中,光照后观察到严重的视网膜损伤,视杆细胞外段(ROS)缩短,外核层(ONL)厚度显著减小。脉络膜毛细血管阻塞。照射后,白化病大鼠的大片区域视网膜色素上皮(RPE)缺失。相比之下,但尽管观察到个体差异,LE 大鼠在强光暴露后 RPE 和视网膜中的细胞损伤要少得多。与对照组相比,ONL 厚度几乎没有变化。LE 大鼠的 ROS 缩短,但效果远小于白化病大鼠。在有色大鼠脉络膜血管中仅发现极小的变化。RPE 显示出一定的毒性损伤,但细胞不像无色动物那样被破坏。照射后 LE 大鼠 RPE 中的黑色素颗粒数量减少。眼部黑色素可保护有色眼睛的视网膜和脉络膜免受光诱导的细胞毒性作用。在瞳孔未扩大的眼睛中可能存在的虹膜黑色素的物理保护作用,在我们的实验设置中似乎不起主要作用。生化机制,如减少细胞内氧化应激,更可能是瞳孔扩大的眼睛中黑色素相关光保护的原因所在。

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